病毒调控应激颗粒形成的策略及应激颗粒对病毒复制的影响

Viruses regulate stress granules formation and the effects of stress granules on virus replication

病毒严格在细胞内寄生,其依赖于宿主细胞的翻译系统进行复制增殖。近年多项研究发现,细胞内核糖核蛋白(RNP)聚集形成的应激颗粒(SG)具有调控病毒复制的功能。病毒感染细胞后,一方面,诱导真核起始因子2α(eIF2α)磷酸化并形成SG,SG通过内部翻译停滞的mRNA抑制病毒蛋白的翻译,或通过内部模式识别受体(PRR)激活宿主天然免疫应答从而影响病毒复制。另一方面,病毒也相应地进化出抑制eIF2α激酶活化、促进eIF2α去磷酸化以及直接破坏SG组成等多种策略抑制SG的形成,以此逃避宿主的免疫清除。此外,病毒还可利用SG来满足自身复制的需要。阐明病毒与SG之间的相互作用关系有利于深入了解病毒的致病机制,为病毒病的防控提供新思路。

Viruses are strictly intracellular parasites and their replication is highly reliant on host cell translation machinery.Recent research showed that stress granule(SG),the aggregation of ribonucleoprotein(RNP),could interfere with viral replication.During virus infection,eukaryotic initiation factor 2α(eIF2α)phosphorylation and SG assembly may be triggered.Meanwhile,mRNA and pattern recognition receptors(PRR)stranded in SG may affect viral replication by inhibiting translation or activating innate immune responses.Accordingly,viruses have developed various strategies,including inhibiting eIF2αphosphorylation,promoting eIF2αdephosphorylation and disrupting SG components directly,to modulate SG formation.In addition,viruses may take advantage of SG to benefit its survival.Further elucidation of the interactions between viruses and SG could help to deepen the understanding of virus pathogenesis and provide new ideas for prevention of virus infections.